Department of Internal Medicine, Catholic University Medical School, Largo Gemelli 8, Rome 00168, Italy.
Int J Mol Sci. 2013 Oct 30;14(11):21525-50. doi: 10.3390/ijms141121525.
In recent decades, oxidative stress has become a focus of interest in most biomedical disciplines and many types of clinical research. Increasing evidence shows that oxidative stress is associated with the pathogenesis of diabetes, obesity, cancer, ageing, inflammation, neurodegenerative disorders, hypertension, apoptosis, cardiovascular diseases, and heart failure. Based on these studies, an emerging concept is that oxidative stress is the "final common pathway" through which the risk factors for several diseases exert their deleterious effects. Oxidative stress causes a complex dysregulation of cell metabolism and cell-cell homeostasis; in particular, oxidative stress plays a key role in the pathogenesis of insulin resistance and β-cell dysfunction. These are the two most relevant mechanisms in the pathophysiology of type 2 diabetes and its vascular complications, the leading cause of death in diabetic patients.
近几十年来，氧化应激已成为大多数生物医学学科和许多类型临床研究的关注焦点。越来越多的证据表明，氧化应激与糖尿病、肥胖症、癌症、衰老、炎症、神经退行性疾病、高血压、细胞凋亡、心血管疾病和心力衰竭的发病机制有关。基于这些研究，一个新出现的概念是，氧化应激是多种疾病的危险因素发挥其有害作用的“共同终末途径”。氧化应激导致细胞代谢和细胞间内稳态的复杂失调；特别是，氧化应激在胰岛素抵抗和β细胞功能障碍的发病机制中起关键作用。这是 2 型糖尿病及其血管并发症病理生理学中两个最相关的机制，也是糖尿病患者死亡的主要原因。
